CVS 238 Heart Failure Flashcards

1
Q

What can you split heart failure into?

A

Right and left sided

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2
Q

What are the features of right sided heart failure?

A

congestion of peripheral tissues –> oedema, ascites, hepatomegaly

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3
Q

What are the features of left sided heart failure?

A

decreased CO and pulmonary congestion orthopnoea, PND, frothy sputum and cough activity intolerances, cyanosis, hypoxia

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4
Q

What can left sided heart failure be split into further?

A

Systolic and diastolic Systolic: insufficient contraction diastolic: insufficient relaxation

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5
Q

What are some causes of systolic dysfunction?

A

Impaired contractility: ischaemia Increased afterload: aortic stenosis/HTN

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6
Q

What is the cause of diastolic dysfunction?

A

impaired filling: hypertrophy, cardiomyopathy, pericardial disease

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7
Q

What are the mechanisms of HF?

A

cardiac muscle necrosis or apoptosis

poor contractility: gene expression changes, changed energy metabolism, changes in calcium handling

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8
Q

How can changes in calcium handling result in HF?

A

depleted stores in the sarcoplasmic reticulum = less release and th. energy to contract = systolic dysfunction impaired reuptake of calcium = diastolic dysfunction

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9
Q

What are the two main mechanisms of compensation in HF?

A

Frank-Starlings law and neurohumoral activation

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10
Q

How does compensation in heart failure work?

A

vasoconstriction to increase TPR venoconstriction to increase CVP and preload increased circulating catecholamines increase RAAS activity to increase blood volume = restoration of CO at the expense of higher filling pressures

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11
Q

What are the two reasons and the type types of ventricular hypertrophy and remodelling in HF?

A

Pressure overload = concentric hypetrophy = diastolic dysfunction Volume overload = eccentric hypertrophy = vicious circle/exacerbation of HF

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12
Q

What is concentric hypetrophy?

A

Increase in number of muscle fibres

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13
Q

What is eccentric hypetrophy?

A

Increase in length of muscle fibres

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14
Q

Why is compensation in HF not good in the long term?

A

It results in a faster deterioration of the muscle to pump against the increased TPR Cardiomegaly from increased filling pressures and oedema from volume expansion

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15
Q

What are the problems as a result of cardiomegaly in HF?

A

Heart has to work harder to generate pressures and enlarged ventricles but valves stay the same- leaky valves

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16
Q

What are ventricular arrhythmias due to in HF?

A

delayed after depolarisations - reentrance circuits in the heart resulting in abnormal release of calcium and a depolarisation after AP

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17
Q

What are the principles of treatment for HF?

A

Decrease cardiac oxygen demand th. work via arterial and veno dilation

decrease stroke volume –> arterial pressures

decreased cardiac dilatation and oedema

decrease arrhythmias

increase coronary perfusion

increase contractility

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18
Q

What drugs will decrease cardiac oxygen demand & increase stroke volume

A

ACEI by decreasing arterial pressures - vasodilators

19
Q

What drugs are useful in oedema?

A

diuretics

20
Q

What drugs increase coronary perfusion and decrease arrhythmias?

A

beta blockers

21
Q

What drug increases heart contractility?

A

digoxin

22
Q

What conditions might mimic heart failure?

A

High output circulatory states: sepsis, anaemia, liver failure, beri-beri, thyrotoxicosis, pagets

23
Q

What is BNP?

A

brain natriuretic peptide - rises in response to myocardial wall stress. high levels in hf despite optimal treatment has a poor prognosis

24
Q

What are the general non-pharmacological managements in HF?

A

monitor weight gain salt-restricted diet limited alcohol intake moderate daily exercise fluid restriction in severe HF

25
Q

How much weight gain in HF would require the patient to self refer and to increase diuretic dose?

A

>2kg in 72hours

26
Q

What are the disease modifying drugs in HF?

A

ACEI ARBS Beta blockers ivabradine

27
Q

How do ACEI work?

A

inhibit ACE so decreased angiontensin 2 and therefore aldosterone - less sodium and water retention, also less vasoconstriction Also inhibits bradykinin breakdown = vasodilation

28
Q

What is the most common side effect of acei?

A

cough and hypotension

29
Q

What are some contraindications of ACEI?

A

bilateral renal artery stenosis, pregnancy, creat> 220, severe AS/HCOM

30
Q

What are ARB’s

A

Angiontensin receptor blockers use last in combination with pretty much all the other heart drugs

31
Q

give some examples of acei?

A

ramipril, perinodopril, captopril

32
Q

give some examples of arbs?

A

candesartan, valsartan

33
Q

What do you give instead to someone with an intolerance to acei/arbs

A

isosobide dinitrate or hydralazine

34
Q

What is ivabradine?

A

drug that acts at the if receptor on the sinus node to slow the heart rate in sinur rhythm - cant be used in AF/not sinus rhythm

35
Q

What is spironolactone?

A

An anti-androgen and pottasium sparing diuretic - common side effect of gynaecomastia

36
Q

What are the symptom relieving drugs in HF?

A

diuretics

37
Q

What are some loop diuretics?

A

furosemide and bumetanide

38
Q

What are the thiazide diuretics?

A

bendroflumethiazide

39
Q

What is a loop diuretic often used in combination with?

A

K sparing diuretic to prevent hypokalaemia

40
Q

What are the surgical options for HF?

A

revascularisation - CABG/PCI treat valvular heart disease - valve replacement cardiac resynchronisation therapy (CRT-P) biventricular implantable defibrillation (CRT-D) heart transplant

41
Q

Lead-in: In the medical management of acute left ventricular failure pair the following
statements with the corresponding drug from the list below. Each drug may be
chosen once, many times or never.

A

1F

2G

3E

4F

5K

42
Q
A

1B

2M

3H

4M

5D

43
Q
A

1K

2L

3D

4F

5B

44
Q
A

1B

2E

3J

4N

5J